I don't think throwing a drowning man a straw is lying. It's just placating those who believe the man isn't really drowning.

You claimed that he knowingly wrote what he did not believe to be true. If you do not count that as "lying" then ... then that goes some way towards explaining your own behavior.

This from Motoo:

"More than a decade and a half ago, in collaboration with Ohta, I enumerated five principles that govern molecular evolution, one of which states that functionally less important molecules or parts of a molecule evolve (in terms of mutant substitutions) faster than more important ones."

Even here Kimura is throwing the neo-Darwinists a bone. He could equally have said that functionally less important parts of a molecule evolve, while important ones don't. After all, this is precisely what his research shows.

So, you once more accuse him of falsehood.

"When this principle was proposed, accompanied by its neutralist explanation, much opposition was voiced by the neo-Darwinian establishment"

You boys got your knickers in a twist.

"... but I am glad to note that it has become a part of common knowledge among molecular biologists

Yes, all evolutionists agree with Kimura. As does he with them.

I was right. Suck it up.

What do you imagine you were right about?

Hey, you can still pretend that selection somehow -magically- evolves the phenotype while leaving the genotype untouched.

I cannot "still" do that because I have never done it.

You were having a hard enough time lying about Kimura's opinions behind his back. Now you are lying to me about my own opinions to my face. How do you think that is going to work out for you?

I have a collection of coins; it consists of only State Celebration quarters. The collection is the result of the random change given me each day. What coins I get every day is a purely random event, yet the collection has only the State Celebration coins.

Anyone so limited that they can only spell a word one way is severely handicapped!

We could discus how random mutation combined with natural selection produces adaptation in a thread where it would be on-topic, but not here. This thread is Wright et al. on the Process of Mutation, and a prerequisite for participation is an understanding of how evolution works.

So you understand that your thinking is fallacious, but you justify it because you believe my thinking is also fallacious. Well, all I've got to say is thank God two wrongs make a right. Oh, wait a minute, they don't

Believing in something you can't prove it doesn't mean it is inevitably fallacious.Innate intelligence is a fact, becouse universal laws is a fact. Just closing eyes before facts is not the cleverest act in the world.

You seem to be having a difficult time understanding that natural selection is not random. It isn't directed, there's no goal, but it is certainly not random.

Of course natural selection is not random. When did i say it? But you believe mutations are. And this the crucial thing in evolution. In my opinion random mutations exist but they are less important in relation to those, which are environment information guided.

If Percy and you really believe that random mutations exist, then you believe that man has been created by pure chance, becouse mutations is the critical factor in evolution.

Selection and mutation are equally important. Mutation is important for creating variability, and it is random with respect to fitness. Selection is important for filtering these variations in phenotype so that the population adapts to their environment over many generations. So which is more important, having variation or adapting to your environment?

As to the Wright paper, the end result is obviously non-random. All of the colonies growing on the plates lacking leucine had a specific mutation. Compare this to the population before plating where only 1 in 500 million had this mutation. That can't happen through chance time after time.

Hey, you can still pretend that selection somehow -magically- evolves the phenotype while leaving the genotype untouched.

Who is claiming that? In fact, this thread is focused on mutations that lead to a change in phenotype. Perhaps you could discuss that?

What the found in the paper is that before plating in the absence of leucine that a specific mutation existed in 1 in every 500 million bacteria. After selection 1 in every 1 had this mutation. How can this occur by chance as you suggest?

Selection and mutation are equally important. Mutation is important for creating variability, and it is random with respect to fitness. Selection is important for filtering these variations in phenotype so that the population adapts to their environment over many generations. So which is more important, having variation or adapting to your environment?

There is no point of disagreeing which of them is most important in evolution.As you say mutation is important for CREATING variability.Natural selection is a filtering mechanism, applying to all types of evolution (by endosymbiosis,random mutations, guided mutations, neural system intervention).This is where we really disagree; the degree of other types of evolution participation and of course manly if there are other types of evolution.

In my opinion random mutations exist but they are less important in relation to those, which are environment information guided

It seems you are having difficulty understanding this issue of random mutations. I can relate. I had some difficulty with it for a while too. I will share some of the things that helped me understand this issue better and maybe it will help you too.

First, I don’t like the term “random” mutations. Not that its wrong or incorrect, I just think it lends some confusion when first trying to understand this subject. I think the term “spontaneous mutations” works better. I think it removed my preconceived notions of what random meant and made it more clear that it is more about “why” mutations occur that makes them “random”. Mutations arise primarily from mistakes in the replication processes (it may even be exclusively because of mistakes – I don’t know of any situation that would not be considered a mistake). A wrong base substitution, aberrant pairing during crossing over, non-disjunction during meiosis, deletions, inversions etc... mistakes in replication.

This paper discusses another source of mutations – single stranded DNA, which may at first seem as though this could be a directed process. Open the DNA, switch some base pairs and off you go. But it is just not that easy. In order for the cell to make the proper substitutions it would need to know what substitutions would produce what effects. There is no know mechanism that could account for that.

One possible mechanism is a type of DNA editing similar to what some eukaryotes use to process mRNA. Starvation could induce production of an RNA template that could be used to edit the sequence in the single stranded DNA being transcribed. But even if such a mechanism did exist, why do only 2 out of 1 billion get the proper mutation? And there was no mention of the number of harmful mutations or neutral mutations (although Taq alluded to it) because those mutations were not the subject of this study. How many harmful or neutral mutations do you suppose there were in that population of 1 billion? A lot more than 2 maybe?

This may not be intuitive in bacteria since any effects of mutations are almost immediately expressed in novel environments. Also, the effects of a mutation affect not only the offspring but the parent cell too. However, you could think of this in a different way. You have in your body right now millions of sperm cells (I assume you are male, if not substitute egg for sperm ). Each of those sperm probably contains at least one mutation. How could your sperm possibly know what mutation your offspring will need to deal with the environment they will be subjected to? There is also no way to specify which sperm will get to fertilize the egg – the first one to the egg wins, essentially a random process too.

Bottom line... mutations are “random” with respect to fitness. They occur spontaneously without respect to whether the organism needs it or not. Of course, organisms have mechanisms that help them deal with their environment, such as the one discussed in this paper – hypermutation of a specific region. There is no known mechanism that allows the bacteria to specify the specific mutation that happens but it does allow them to “try” many different mutations and the end result is the population gets “just the right mutation” they need to survive.

Its been a while since I have posted on this forum, but I have a break for about a month and thought I would spend a little time here.

I do not disagree with the major premise of the thread that mutations are random with respect to fitness. I do, however, have some questions about the Wright et al. paper and would like to discuss them.

1. The authors do seem to be arguing for at least a form of directed mutation.

quote: RNA polymerase pausing is thought to be a mechanism that could determine the site of mutagenesis

Specifying the site of a mutation would certainly increase the likelihood of getting the “needed” mutation. Wouldn’t you consider this a type of directed mutation? I realize that even at a specified site the exact mutation would be random, but directing a mutagen to a specific site would definitely improve the odds.

quote: In our view, these studies demonstrating enhanced mutation rates as a result of artificially induced transcription are all examples of specifically induced mutations.

I realize that “specifically induced mutations” is not the same thing as directed mutations. But perhaps this has caused some confusion with those in this thread that have trouble with mutations being random. I am unclear as to what their actual hypothesis was in this paper. It seems to be derepression-induced hypermutation being the link between mutations and environmental stress. Is that a fair summary of their position?

2. The authors state that

quote: ssDNA is more vulnerable to mutagenesis than double-stranded DNA.

I guess I fail to see how this would be. While transcription is going on wouldn’t the template strand be shielded from mutations? Perhaps the non-template strand would be vulnerable but this would have little or no effect. When transcription ended, the DNA would zip back up, polymerase would detect the misplaced bases and repair (at least the majority). Perhaps they would “repair” the wrong strand and end up with a mutation, but I don’t really see that as hypermutation. In addition, when DNA opens up into single strand, it adds proteins (I don’t recall the name for them) to stabilize and protect the ssDNA. So I don’t really see how transcription alone is cause for hypermutation. I did not see where they gave anymore explanation for increased mutation rate besides increased transcription.

3. In the OP you stated:

With respect to the paper, I will attempt to demonstrate that the same mechanisms that produce reversions in leuB- organisms will also cause deleterious mutations in very important and vital genes as well as mutations which do not change the fitness of offspring.

I did not see where you did this. Not that I doubt that the premise would be true, but I don’t think the data in the paper supports rates of deleterious or neutral mutations. It seems that leu- or reversion mutations were all that were distinguish. How were you going to accomplish this statement in your OP? Is there data I missed? It would seem that the total rate of mutation would have been important to this study. It would help establish hypermutation. It looks as if mutation (reversions) rates doubled, maybe quadrupled? Is that right? Not exactly “hyper” IMHO. So could it could be only reversions that increased and not total mutation rate? If so, it could indicate that something was indeed directing mutations to a specific site (the reversion site).